PMID- 26159804
OWN - NLM
STAT- MEDLINE
DCOM- 20160617
LR  - 20191113
IS  - 2211-5374 (Electronic)
VI  - 4
IP  - 1
DP  - 2015
TI  - Temporal Expression of miRNAs in Laser Capture Microdissected Palate Medial Edge 
      Epithelium from Tgfbeta3(-/-) Mouse Fetuses.
PG  - 64-71
AB  - Clefting of the secondary palate is the most common birth defect in humans. 
      Midline fusion of the bilateral palatal processes is thought to involve 
      apoptosis, epithelial to mesenchymal transition, and cell migration of the medial 
      edge epithelium (MEE), the specialized cells of the palate that mediate fusion of 
      the palatal processes during fetal development. Data presented in this manuscript 
      are the result of analyses designed to identify microRNAs that are expressed and 
      regulated by TGFbeta3 in developing palatal MEE. The expression of 7 microRNAs was 
      downregulated and 1 upregulated in isolated MEE from wildtype murine fetuses on 
      gestational day (GD) 13.5 to GD14.5 (prior to and during epithelial fusion of the 
      palatal processes, respectively). Among this group were miRNAs linked to 
      apoptosis (miR-378) and epithelial to mesenchymal transformation (miR-200b, 
      miR-205, and miR-93). Tgfbeta3(-/-) fetuses, which present with a complete and 
      isolated cleft of the secondary palate, exhibited marked dysregulation of 
      distinct miRNAs both in the palatal MEE and mesenchyme when compared to 
      comparable wild-type tissue. These included, among others, miRNAs known to affect 
      apoptosis (miR-206 and miR-186). Dysregulation of miRNAs in the mesenchyme 
      underlying the palatal MEE of Tgfbeta3(-/-) fetuses is also discussed in relation to 
      epithelial-mesenchymal transformation of the MEE. These results are the first 
      systematic analysis of the expression of microRNAs in isolated fetal palatal 
      epithelium and mesenchyme. Moreover, analysis of the Tgfbeta3 knockout mouse model 
      has enabled identification of miRNAs with altered expression that may contribute 
      to the cleft palate phenotype.
FAU - Warner, Dennis
AU  - Warner D
FAU - Ding, Jixiang
AU  - Ding J
FAU - Mukhopadhyay, Partha
AU  - Mukhopadhyay P
FAU - Brock, Guy
AU  - Brock G
FAU - Smolenkova, Irina A
AU  - Smolenkova IA
FAU - Seelan, Ratnam S
AU  - Seelan RS
FAU - Webb, Cindy L
AU  - Webb CL
FAU - Wittliff, James L
AU  - Wittliff JL
FAU - Greene, Robert M
AU  - Greene RM
AD  - Department of Molecular, Cellular, and Craniofacial Biology, University of 
      Louisville Birth Defects Center, 501 S. Preston St, suite 350, University of 
      Louisville, Louisville, Kentucky, 40202, USA. dr.bob.greene@gmail.com.
FAU - Pisano, M Michele
AU  - Pisano MM
LA  - eng
GR  - DE018215/DE/NIDCR NIH HHS/United States
GR  - HD053509/HD/NICHD NIH HHS/United States
GR  - P20 RR017702/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United Arab Emirates
TA  - Microrna
JT  - MicroRNA (Shariqah, United Arab Emirates)
JID - 101631045
RN  - 0 (MicroRNAs)
RN  - 0 (Transforming Growth Factor beta3)
SB  - IM
MH  - Animals
MH  - Cleft Palate/*embryology/genetics
MH  - Epithelium/embryology/metabolism
MH  - Fetus/embryology/metabolism
MH  - Gene Deletion
MH  - Gene Expression Regulation, Developmental
MH  - Laser Capture Microdissection
MH  - Mice/*embryology/genetics
MH  - Mice, Knockout
MH  - MicroRNAs/*genetics
MH  - Palate/*embryology/metabolism
MH  - Transforming Growth Factor beta3/*genetics
EDAT- 2015/07/15 06:00
MHDA- 2016/06/18 06:00
CRDT- 2015/07/11 06:00
PHST- 2015/04/04 00:00 [received]
PHST- 2015/07/01 00:00 [revised]
PHST- 2015/07/07 00:00 [accepted]
PHST- 2015/07/11 06:00 [entrez]
PHST- 2015/07/15 06:00 [pubmed]
PHST- 2016/06/18 06:00 [medline]
AID - MIRNA-EPUB-68745 [pii]
AID - 10.2174/2211536604666150710125743 [doi]
PST - ppublish
SO  - Microrna. 2015;4(1):64-71. doi: 10.2174/2211536604666150710125743.